Research
The transformation of normal cells into cancer cells and their subsequent acquisition of therapeutic resistance cannot be fully explained by genetic mutations alone; instead, epigenetic and epitranscriptomic dysregulation plays a central role in these processes.
Accordingly, our lab aims to elucidate the molecular mechanisms by which epigenetic and epitranscriptomic regulatory pathways are rewired in cancer, and how these alterations drive malignant transformation and therapeutic resistance.
Mechanistic regulation of oncogenic RNA splicing
In cancer and therapy-resistant states, RNA processing is extensively reprogrammed, and oncogenic RNA splicing plays a critical role in cancer cell survival and adaptation.
My research focuses on elucidating the molecular mechanisms by which RNA-binding proteins (RBPs) and other regulatory factors control oncogenic RNA splicing, as well as identifying aberrant splicing events that are selectively enriched in malignant conditions.
Coupling between epigenetic–transcriptional networks and RNA splicing
Alterations in RNA splicing are not merely post-transcriptional events, but are tightly coupled to changes in the epigenetic landscape and molecular interaction networks mediated by transcription factors and other regulatory elements.
This research aims to define how transcriptional regulation, chromatin organization, and RNA processing are integrated into a coordinated regulatory axis in cancer.
Identification of novel regulatory factors through CRISPR-based screening
To uncover essential regulators of cancer progression and therapeutic resistance, I plan to employ CRISPR-based functional screening approaches.
This strategy will enable the identification of novel regulatory factors within epigenetic and epitranscriptomic networks, followed by mechanistic characterization of their roles in malignant gene regulation.
